Feline physeal dysplasia is a syndrome characterized by a progressive dis-placement of the capital femoral epiphysis in relation to the proximal femoral metaphysis through the growth plate, resulting in a fracture in the growth plate. The displacement is made possible due to wider than normal and open growth plates in the proximal femur. Feline fyseal dysplasia is also referred to as “slipped capital femoral epiphysis” (SCFE), “feline capital physeal dys-plasia syndrome” and “spontaneous femoral capital physeal fracture”.

Those mainly afflicted are adult, neutered and overweight male cats but the syndrome is also seen in spayed female cats and in intact male and female cats. One of the distinguishing features of SCFE is that the fracture of the growth plate is atraumatic. Characteristic features histologically are widening of the growth plate to approximately twice its normal size and randomly scat-tered chondrocytes in clusters, surrounded by large amounts of extracellular matrix (ECM).

Bone sclerosis and osteolysis may also be seen in the trabecular metaph-yseal bone, and most likely represent secondary changes to fracturing of the growth plate. The pathogenesis of SCFE is not known, most likely it is a mul-tifactorial syndrome with predisposing factors such as heredity, overweight, endocrine imbalance, neutering and sex.

This review targets the question whether or not neutering at an early-age in cats increases the risk of SCFE. A survey of the growth plate and some of its regulatory mechanisms is also included. The growth plate is under the in-fluence of several different kind of signalling molecules. Some exert their effect systemically, others locally and some works both ways. Examples of substances that influences the growth plate are oestrogen, leptin, Insulin-like growth factor (IGF)-1, Growth hormone (GH), Runx2 and transforming growth factor (TGF)-β. The concentration of the substance is also of im-portance. For instance, oestrogen in low concentrations stimulates growth whereas it in high concentration stimulates closure of the growth plate. The exact mechanism of epiphyseal fusion is not known.

Neutering of cats delay the fusion of the growth plate (delayed fusion of the growth plate being one characteristic of SCFE). The delay is seen regard-less if the cat is neutered at an age of seven weeks or seven months. Studies shows, that neutering prior to seven months of age does not increase the risk of developing SCFE, despite the fact neutering leads to a delayed fusion of the growth plate. The conclusion of this review is instead that SCFE probably has a genetic background.